Evolution of virulence in malaria.

Abstract

The pathogenesis of severe malarial disease is not yet fully understood. It is clear that host immunopathology plays a central role, and a recent paper in BMC Evolutionary Biology suggests that the ability of the parasite to stimulate interleukin-10 production is a major factor and speculates on its impact on the coevolution of host and parasite.

Differential binding of the P. falciparum erythrocyte membrane protein (PfEMP1) to host tissues. The parasite protein PfEMP1 is expressed on the surface of infected red blood cells and binds to adhesion proteins chiefly on endothelial cells. Different variants of PfEMP1 bind to adhesion proteins expressed on different endothelia and lead to different disease phenotypes. CR1, ICAM-1, CSA and CD36 are all distinct cellular adhesion molecules. The figure is Figure U11-1.2 from the online update to Immunity: The Immune Response in Infectious and Inflammatory Disease by DeFranco, Locksley and Robertson (New Science Press, London, 2007) [].